| First Author | Chen F | Year | 2018 |
| Journal | Cell Rep | Volume | 25 |
| Issue | 10 | Pages | 2775-2783.e3 |
| PubMed ID | 30517865 | Mgi Jnum | J:271213 |
| Mgi Id | MGI:6278472 | Doi | 10.1016/j.celrep.2018.11.038 |
| Citation | Chen F, et al. (2018) B Cells Produce the Tissue-Protective Protein RELMalpha during Helminth Infection, which Inhibits IL-17 Expression and Limits Emphysema. Cell Rep 25(10):2775-2783.e3 |
| abstractText | Emphysema results in destruction of alveolar walls and enlargement of lung airspaces and has been shown to develop during helminth infections through IL-4R-independent mechanisms. We examined whether interleukin 17A (IL-17A) may instead modulate development of emphysematous pathology in mice infected with the helminth parasite Nippostrongylus brasiliensis. We found that transient elevations in IL-17A shortly after helminth infection triggered subsequent emphysema that destroyed alveolar structures. Furthermore, lung B cells, activated through IL-4R signaling, inhibited early onset of emphysematous pathology. IL-10 and other regulatory cytokines typically associated with B regulatory cell function did not play a major role in this response. Instead, at early stages of the response, B cells produced high levels of the tissue-protective protein, Resistin-like molecule alpha (RELMalpha), which then downregulated IL-17A expression. These studies show that transient elevations in IL-17A trigger emphysema and reveal a helminth-induced immune regulatory mechanism that controls IL-17A and the severity of emphysema. |
